Non-Perturbative Scales in Soft Hadronic Collisions at High Energies

We investigate the role of nonperturbative quark-gluon dynamics in soft high energy processes. In order to reproduce differential and total cross sections for elastic proton-proton and proton-antiproton-scattering at high energy and small momentum transfer it turns out that we need two scales, the gluonic correlation length and a confinement scale. We find a small gluonic correlation length, a = 0.2 fm, in accordance with recent lattice QCD results.Comment: 8 pages,latex, 2 figures uuencode

High energy parton-parton amplitudes from lattice QCD and the stochastic vacuum model

Making use of the gluon gauge-invariant two-point correlation function, recently determined by numerical simulation on the lattice in the quenched approximation and the stochastic vacuum model, we calculate the elementary (parton-parton) amplitudes in both impact-parameter and momentum transfer spaces. The results are compared with those obtained from the Kr\"{a}mer and Dosch ansatz for the correlators. Our main conclusion is that the divergences in the correlations functions suggested by the lattice calculations do not affect substantially the elementary amplitudes. Phenomenological and semiempirical information presently available on elementary amplitudes is also referred to and is critically discussed in connection with some theoretical issues.Comment: Text with 11 pages in LaTeX (twocolumn form), 10 figures in PostScript (psfig.tex used). Replaced with changes, Fig.1 modified, two references added, some points clarified, various typos corrected. Version to appear in Phys. Rev.

Scaling violations: Connections between elastic and inelastic hadron scattering in a geometrical approach

Starting from a short range expansion of the inelastic overlap function, capable of describing quite well the elastic pp and $\bar{p}p$ scattering data, we obtain extensions to the inelastic channel, through unitarity and an impact parameter approach. Based on geometrical arguments we infer some characteristics of the elementary hadronic process and this allows an excellent description of the inclusive multiplicity distributions in $pp$ and $\bar{p}p$ collisions. With this approach we quantitatively correlate the violations of both geometrical and KNO scaling in an analytical way. The physical picture from both channels is that the geometrical evolution of the hadronic constituents is principally reponsible for the energy dependence of the physical quantities rather than the dynamical (elementary) interaction itself.Comment: 16 pages, aps-revtex, 11 figure

Group B Streptococcal β-Hemolysin/Cytolysin Directly Impairs Cardiomyocyte Viability and Function

BACKGROUND: Group B Streptococcus (GBS) is a leading cause of neonatal sepsis where myocardial dysfunction is an important contributor to poor outcome. Here we study the effects of the GBS pore-forming beta-hemolysin/cytolysin (Bh/c) exotoxin on cardiomyocyte viability, contractility, and calcium transients. METHODOLOGY/PRINCIPAL FINDINGS: HL-1 cardiomyocytes exposed to intact wild-type (WT) or isogenic Deltabeta h/c mutant GBS, or to cell-free extracts from either strain, were assessed for viability by trypan blue exclusion and for apoptosis by TUNEL staining. Functionality of exposed cardiomyocytes was analyzed by visual quantitation of the rate and extent of contractility. Mitochondrial membrane polarization was measured in TMRE-loaded cells exposed to GBS beta h/c. Effects of GBS beta h/c on calcium transients were studied in fura-2AM-loaded primary rat ventricular cardiomyocytes. Exposure of HL-1 cardiomyocytes to either WT GBS or beta h/c extracts significantly reduced both rate and extent of contractility and later induced necrotic and apoptotic cell death. No effects on cardiomyocyte viability or function were observed after treatment with Deltabeta h/c mutant bacteria or extracts. The beta h/c toxin was associated with complete and rapid loss of detectable calcium transients in primary neonatal rat ventricular cardiomyocytes and induced a loss of mitochondrial membrane polarization. These effects on viability and function were abrogated by the beta h/c inhibitor, dipalmitoyl phosphatidylcholine (DPPC). CONCLUSIONS/SIGNIFICANCE: Our data show a rapid loss of cardiomyocyte viability and function induced by GBS beta h/c, and these deleterious effects are inhibited by DPPC, a normal constituent of human pulmonary surfactant.. These findings have clinical implications for the cardiac dysfunction observed in neonatal GBS infections

The response of the host microcirculation to bacterial sepsis: Does the pathogen matter?

Sepsis results from the interaction between a host and an invading pathogen. The microcirculatory dysfunction is now considered central in the development of the often deadly multiple organ dysfunction syndrome in septic shock patients. The microcirculatory flow shutdown and flow shunting leading to oxygen demand and supply mismatch at the cellular level and the local activation of inflammatory pathways resulting from the leukocyte-endothelium interactions are both features of the sepsis-induced microcirculatory dysfunction. Although the host response through the inflammatory and immunologic response appears to be critical, there are also evidences that Gram-positive and Gram-negative bacteria can exert different effects at the microcirculatory level. In this review we discuss available data on the potential bacterial-specific microcirculatory alterations observed during sepsis

Anaplastic Lymphoma Kinase Is Required for Neurogenesis in the Developing Central Nervous System of Zebrafish

10.1371/journal.pone.0063757PLoS ONE85

Human Cytomegalovirus IE1 Protein Elicits a Type II Interferon-Like Host Cell Response That Depends on Activated STAT1 but Not Interferon-γ

Human cytomegalovirus (hCMV) is a highly prevalent pathogen that, upon primary infection, establishes life-long persistence in all infected individuals. Acute hCMV infections cause a variety of diseases in humans with developmental or acquired immune deficits. In addition, persistent hCMV infection may contribute to various chronic disease conditions even in immunologically normal people. The pathogenesis of hCMV disease has been frequently linked to inflammatory host immune responses triggered by virus-infected cells. Moreover, hCMV infection activates numerous host genes many of which encode pro-inflammatory proteins. However, little is known about the relative contributions of individual viral gene products to these changes in cellular transcription. We systematically analyzed the effects of the hCMV 72-kDa immediate-early 1 (IE1) protein, a major transcriptional activator and antagonist of type I interferon (IFN) signaling, on the human transcriptome. Following expression under conditions closely mimicking the situation during productive infection, IE1 elicits a global type II IFN-like host cell response. This response is dominated by the selective up-regulation of immune stimulatory genes normally controlled by IFN-γ and includes the synthesis and secretion of pro-inflammatory chemokines. IE1-mediated induction of IFN-stimulated genes strictly depends on tyrosine-phosphorylated signal transducer and activator of transcription 1 (STAT1) and correlates with the nuclear accumulation and sequence-specific binding of STAT1 to IFN-γ-responsive promoters. However, neither synthesis nor secretion of IFN-γ or other IFNs seems to be required for the IE1-dependent effects on cellular gene expression. Our results demonstrate that a single hCMV protein can trigger a pro-inflammatory host transcriptional response via an unexpected STAT1-dependent but IFN-independent mechanism and identify IE1 as a candidate determinant of hCMV pathogenicity